cyclin-d1 and Cleft-Lip
cyclin-d1 has been researched along with Cleft-Lip* in 3 studies
Other Studies
3 other study(ies) available for cyclin-d1 and Cleft-Lip
Article | Year |
---|---|
Chloroquine regulates the proliferation and apoptosis of palate development on mice embryo by activating P53 through blocking autophagy in vitro.
Cleft lip and palate is one of the most frequent congenital developmental defects. Autophagy is a highly conserved process of cell self-degradation in eukaryotes, involving multiple biological processes in which chloroquine (CQ) is the most common inhibitor. However, whether CQ affects and how it affects palate development is unknown. Mouse embryonic palatal cells (MEPCs) were treated with CQ to observe cell viability, apoptosis, migration, osteogenic differentiation by cell proliferation assay, flow cytometric analysis, scratch assay, and alizarin red staining. PI staining was used to measure cell cycle distribution. Immunofluorescence (IF) assay and transmission electron microscopy were used to detect autophagosomes. The autophagy-related factors (LC3 and P62), apoptosis-related markers (P53, caspase-3 cleaved caspase-3, BAX, and BCL-2), and cell cycle-related proteins (P21, CDK2, CDK4, cyclin D1, and cyclin E) were all measured by western blot. CQ inhibited the proliferation of MEPCs by arresting the G0/G1 phase of the cell cycle in a concentration- and time-dependent manner with cell cycle-related proteins P21 upregulated and CDK2, CDK4, cyclin D1, and cyclin E downregulated. Then we detected CQ also induced cell apoptosis in a dose-dependent manner by decreasing the BCL-2/BAX ratio and increasing cleaved caspase-3. Next, it was investigated that migration and osteogenesis of MEPCs decreased with CQ treatment in a dose-dependent manner. Meanwhile, CQ blocked the autophagy pathway by upregulating LC3II and P62 expressions which activated the P53 pathway. CQ activates P53 which affects MEPC biological characteristics by changing the proliferation and apoptosis of MEPCs through inhibiting autophagy. Topics: Animals; Apoptosis; Autophagy; bcl-2-Associated X Protein; Biological Phenomena; Caspase 3; Cell Line, Tumor; Cell Proliferation; Chloroquine; Cleft Lip; Cleft Palate; Cyclin D1; Cyclin E; Mice; Osteogenesis; Rodent Diseases; Tumor Suppressor Protein p53 | 2022 |
Transforming growth factor-beta3 promotes mesenchymal cell proliferation and angiogenesis mediated by the enhancement of cyclin D1, Flk-1, and CD31 gene expression during CL/Fr mouse lip fusion.
Cleft lip with or without cleft palate is the most common congenital anomaly in the craniofacial region. Knowledge of the molecular mechanisms behind normal lip fusion can contribute to better intervention and improved functional clinical outcome. Transforming growth factor-beta3 (TGF-beta3) has been implicated in lip morphogenesis. Therefore, we hypothesized that TGF-beta3 functions during lip fusion through regulation of angiogenesis and mesenchymal cell cycle progression during early developmental stages.. To test this hypothesis we used the CL/Fraser mouse model, which has a high incidence of cleft lip. Lips isolated from embryonic day (ED) 11.5 mouse embryos were allowed to develop in serum-free organ cultures in the presence or absence of TGF-beta3. The lips that developed in these cultures fused in 2 days.. During normal development, we detected positive immunoreactions for TGF-beta3 at the site of fusion. We also detected mesenchymal cells that were immunopositive for Flk-1 and CD31, which are markers for endothelial cell precursors. Exogenous TGF-beta3 accelerated lip fusion in culture. This enhancement was associated with an increase in the number of capillary blood vessels in the lips cultured in the presence of TGF-beta3, in comparison with controls. In tandem, TGF-beta3 increased the level of expression of both Flk-1 and CD31. Our data suggest that an elevated level of TGF-beta3 may promote angiogenesis in developing lips that is mediated by increased Flk-1 and CD31 expression. We also detected increased cyclin D1 expression (a marker for cell proliferation) in the presence of TGF-beta3, which suggests that TGF-beta3 promoted cell proliferation.. TGF-beta3 promoted cell proliferation and angiogenesis in lip mesenchymal tissues. These events led to enhanced lip fusion in the presence of TGF-beta3. Topics: Animals; Cell Proliferation; Cleft Lip; Cyclin D1; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression Regulation, Developmental; Mesoderm; Mice; Mice, Mutant Strains; Neovascularization, Physiologic; Organ Culture Techniques; Platelet Endothelial Cell Adhesion Molecule-1; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Transforming Growth Factor beta; Transforming Growth Factor beta3; Vascular Endothelial Growth Factor Receptor-2 | 2005 |
TGF-beta-3 promotes scarless repair of cleft lip in mouse fetuses.
TGF-beta3 mediates epithelial-mesenchymal transformation during normal fusion of lip and palate, but how TGF-beta3 functions during cleft lip repair remains unexplored. We hypothesize that TGF-beta3 promotes fetal cleft lip repair and fusion by increasing the availability of mesenchymal cells. In this investigation, we demonstrated that cleft lips in mouse fetuses were repaired by fetal surgery, producing scarless fusion. At the site of the operation, we first observed an infusion of platelets expressing TGF-beta3, followed by increased expression of cyclin D1 and tenascin-C, and coupled with increased mesenchymal cell proliferation. In an ex vivo serumless culture system, cleft lip explants fused in the presence of exogenous TGF-beta3. Cultured lips also showed up-regulation in cyclin D1 and tenascin-C expression. These findings suggest that microsurgical repair of cleft lip in the fetus that produced scarless fusion is mediated by TGF-beta3 regulation of mesenchymal cell proliferation and migration at the site of repair. Topics: Animals; Antimetabolites; Blood Platelets; Bromodeoxyuridine; Cell Division; Cell Movement; Cicatrix; Cleft Lip; Culture Media, Serum-Free; Cyclin D1; Epithelium; Fetal Diseases; Fetus; Immunohistochemistry; Mesoderm; Mice; Microsurgery; Organ Culture Techniques; Platelet Count; Reverse Transcriptase Polymerase Chain Reaction; Tenascin; Transforming Growth Factor beta; Transforming Growth Factor beta3; Up-Regulation | 2002 |